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Abstract
Intercellular communication between vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) is essential for the maintenance of vascular homeostasis. The presence of exosomes, a recently discovered player in vascular cell communication, has been associated with vascular disease progression. However, the detailed mechanism of how the signal mediated by exosomes affects the function of vascular cells during vascular pathogenesis is yet to be further understood. In this study, we investigated the expression of exosomal microRNAs (miRNAs) secreted by VSMCs and their functional relevance to ECs in pathogenesis, including their role in processes such as platelet-derived growth factor (PDGF) stimulation. We observed that PDGF stimulation contributes to a change in exosomal miRNA release from VSMCs; specifically, miR-1246, miR-182, and miR-486 were deficient in exosomes derived from PDGF-stimulated VSMCs. The reduced miRNA expression in these exosomes is associated with an increase in EC migration. These findings increase our understanding of exosome-mediated crosstalk between vascular cells under a pathological condition.
Highlights
Arterial injury stimulates the production of growth factors, such as platelet-derived growth factor (PDGF) by platelets and a variety of cellular elements associated with the vessel wall
As phenotypic modulation of vascular smooth muscle cells (VSMCs) is essential for the maintenance of vascular homeostasis and pathogenesis, we hypothesized that the signaling effects generated by exosomes secreted by VSMCs under PDGF stimulation might differ from those exerted by exosomes derived from untreated cells
To investigate whether pulmonary artery smooth muscle cells (PASMC)-derived exosomes exposed to a PDGF signal play a regulatory role in the modulation of pulmonary artery endothelial cells (PAEC), we isolated exosomes from a PASMC medium following 40 ng/mL PDGF-BB
Summary
Arterial injury stimulates the production of growth factors, such as platelet-derived growth factor (PDGF) by platelets and a variety of cellular elements associated with the vessel wall. Growth factor production induces a phenotypic change in vascular smooth muscle cells (VSMC) through a conversion of their state from a quiescent, “contractile”, to a proliferative, “synthetic” This change is characterized by cell proliferation, migration, and secretion of matrix [1]. Aberrant PDGF signaling is implicated in vascular remodeling, a complex pathological process of the vascular system, and contributes to a range of vascular pathologies including restenosis, atherosclerosis, and pulmonary hypertension [2,3] This pathogenesis is characterized by dysfunction in major aspects of vasculature regulation, including abnormal proliferation, migration and apoptosis of endothelial cells (EC) and VSMCs. As intercellular communication is essential for the maintenance of tissue homeostasis and disease prevention, understanding the means of interaction between PDGF-modulated VSMCs and ECs might provide important insight into the development of vascular pathogenesis
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